ArticlePsoriasis (Auckland, N.Z.)2019
Increased dermal expression of chromatin-associated protein HMGB1 and concomitant T-cell expression of the DNA RAGE in patients with psoriasis vulgaris.
Article in Psoriasis (Auckland, N.Z.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- NMI promotes the secretion of IL-17 and exacerbates psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Enhancement of Psoriasis Treatment by Phellodendri Chinensis Cortex Carbon Dots (PCC-CDs) Through Modulation of the HMGB1/TLR4/MAPK/NF-κB Pathway.International journal of nanomedicine · 2026Article
- HMGB1: new biomarker and therapeutic target of autoimmune and autoinflammatory skin diseases.Frontiers in immunology · 2025Review
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Damage-Associated Molecular Patterns, a Class of Potential Psoriasis Drug Targets.International journal of molecular sciences · 2024Review
- HMGB1/RAGE Signaling Regulates Th17/IL-17 and Its Role in Bronchial Epithelial-Mesenchymal Transformation.Current molecular medicine · 2024Article
- Etanercept ameliorates psoriasis progression through regulating high mobility group box 1 pathway.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023Article
- Clinical application of serum biomarkers for detecting and monitoring of chronic plaque psoriasis.Frontiers in molecular biosciences · 2023Review
- Knockout of high-mobility group box 1 in B16F10 melanoma cells induced host immunity-mediated suppression of in vivo tumor growth.Medical oncology (Northwood, London, England) · 2022Article
- HMGB-1 in Psoriasis.Biomolecules · 2021Article
- Alarmins HMGB1, IL-33, S100A7, and S100A12 in Psoriasis Vulgaris.Mediators of inflammation · 2020Article
- Johnny on the Spot-Chronic Inflammation Is Driven by HMGB1.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePsoriasis vulgaris (PV) is an autoimmune-related chronic inflammatory disease of the skin, with both vascular and metabolic effects. Aggravating factors have been identified that initiate and maintain inflammation, including expression of Th1-, Th17-, and Th22-cell derived cytokines. Recently, we showed that the evolutionarily ancient and highly conserved damage-associated molecular pattern molecule "high mobility group box 1 (HMGB1)" is significantly increased in the serum of PV patients with disease progression and is decreased under standard therapies. MATERIALS AND
methodsTo better understand the role of HMGB1 in the pathogenesis of PV, we recruited 22 untreated psoriatic patients with either mild or severe disease, defined by the Psoriasis Area Severity Index. We assessed HMGB1 and receptor for advanced glycation end products (RAGE) expression in the skin by immunohistochemistry and analyzed the immune-phenotype of Treg and Th17 cells by flow cytometry.
resultsWe found increased staining for HMGB1 in the dermis of psoriatic plaques in comparison to uninvolved skin of patients with PV. In addition, the major histocompatibility complex class III-encoded DNA and HMGB1 RAGE, induced by HMGB1, were highly expressed on psoriatic CD8+ T cells and CD4+ Treg. High expression of HMGB1 in the lesional skin was associated with even higher expression of its receptor, RAGE, on the cell surface of keratino-cytes in patients with severe PV.
conclusionThe presence of HMGB1 and RAGE signaling may impact orchestration of chronic inflammation in PV which might have implications for Treg and Th17 cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.